Bibliografie tematiche / Cyclomodulin

Letteratura scientifica selezionata sul tema "Cyclomodulin"

Autore: Grafiati
Pubblicato: 6 luglio 2024

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Articoli di riviste sul tema "Cyclomodulin":

1

Markelova, Natalia N., Elena F. Semenova, Olga N. Sineva e Vera S. Sadykova. "The Role of Cyclomodulins and Some Microbial Metabolites in Bacterial Microecology and Macroorganism Carcinogenesis". International Journal of Molecular Sciences 23, n. 19 (3 ottobre 2022): 11706. http://dx.doi.org/10.3390/ijms231911706.

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Abstract (sommario):
A number of bacteria that colonize the human body produce toxins and effectors that cause changes in the eukaryotic cell cycle—cyclomodulins and low-molecular-weight compounds such as butyrate, lactic acid, and secondary bile acids. Cyclomodulins and metabolites are necessary for bacteria as adaptation factors—which are influenced by direct selection—to the ecological niches of the host. In the process of establishing two-way communication with the macroorganism, these compounds cause limited damage to the host, despite their ability to disrupt key processes in eukaryotic cells, which can lead to pathological changes. Possible negative consequences of cyclomodulin and metabolite actions include their potential role in carcinogenesis, in particular, with the ability to cause DNA damage, increase genome instability, and interfere with cancer-associated regulatory pathways. In this review, we aim to examine cyclomodulins and bacterial metabolites as important factors in bacterial survival and interaction with the host organism to show their heterogeneous effect on oncogenesis depending on the surrounding microenvironment, pathological conditions, and host genetic background.
2

Nouri, Roghayeh, Alka Hasani, Kourosh Masnadi Shirazi, Mohammad Reza Alivand, Bita Sepehri, Simin Sotoudeh, Fatemeh Hemmati, Afshin Fattahzadeh, Babak Abdinia e Mohammad Ahangarzadeh Rezaee. "Mucosa-Associated Escherichia coli in Colorectal Cancer Patients and Control Subjects: Variations in the Prevalence and Attributing Features". Canadian Journal of Infectious Diseases and Medical Microbiology 2021 (9 novembre 2021): 1–8. http://dx.doi.org/10.1155/2021/2131787.

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Accumulating evidence indicates that specific strains of mucosa-associated Escherichia coli (E. coli) can influence the development of colorectal carcinoma. This study aimed to investigate the prevalence and characterization of mucosa-associated E. coli obtained from the colorectal cancer (CRC) patients and control group. At two referral university-affiliated hospitals in northwest Iran, 100 patients, 50 with CRC and 50 without, were studied over the course of a year. Fresh biopsy specimens were used to identify mucosa-associated E. coli isolates after dithiothreitol mucolysis. To classify the E. coli strains, ten colonies per sample were typed using enterobacterial repetitive intergenic consensus-based PCR (ERIC-PCR). The strains were classified into phylogroups using the quadruplex PCR method. The PCR method was used to examine for the presence of cyclomodulin, bfp, stx1, stx2, and eae-encoding genes. The strains were tested for biofilm formation using the microtiter plate assay. CRC patients had more mucosa-associated E. coli than the control group ( p < 0.05 ). Enteropathogenic Escherichia coli (EPEC) was also found in 23% of CRC strains and 7.1% of control strains ( p < 0.05 ). Phylogroup A was predominant in control group specimens, while E. coli isolates from CRC patients belonged most frequently to phylogroups D and B2. Furthermore, the frequency of cyclomodulin-encoding genes in the CRC patients was significantly higher than the control group. Around 36.9% of E. coli strains from CRC samples were able to form biofilms, compared to 16.6% E. coli strains from the control group ( p < 0.05 ). Noticeably, cyclomodulin-positive strains were more likely to form biofilm in comparison to cyclomodulin-negative strains ( p < 0.05 ). In conclusion, mucosa-associated E. coli especially cyclomodulin-positive isolates from B2 and D phylogroups possessing biofilm-producing capacity colonize the gut mucosa of CRC patients.
3

Mezerová, Kristýna, Lubomír Starý, Pavel Zbořil, Ivo Klementa, Martin Stašek, Petr Špička, Pavel Skalický e Vladislav Raclavský. "Cyclomodulins and Hemolysis in E. coli as Potential Low-Cost Non-Invasive Biomarkers for Colorectal Cancer Screening". Life 11, n. 11 (31 ottobre 2021): 1165. http://dx.doi.org/10.3390/life11111165.

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The frequent occurrence of E. coli positive for cyclomodulins such as colibactin (CLB), the cytotoxic necrotizing factor (CNF), and the cytolethal distending factor (CDT) in colorectal cancer (CRC) patients published so far provides the opportunity to use them as CRC screening markers. We examined the practicability and performance of a low-cost detection approach that relied on culture followed by simplified DNA extraction and PCR in E. coli isolates recovered from 130 CRC patients and 111 controls. Our results showed a statistically significant association between CRC and the presence of colibactin genes clbB and clbN, the cnf gene, and newly, the hemolytic phenotype of E. coli isolates. We also observed a significant increase in the mean number of morphologically distinct E. coli isolates per patient in the CRC cohort compared to controls, indicating that the cyclomodulin-producing E. coli strains may represent potentially preventable harmful newcomers in CRC patients. A colibactin gene assay showed the highest detection rate (45.4%), and males would benefit from the screening more than females. However, because of the high number of false positives, practical use of this marker must be explored. In our opinion, it may serve as an auxiliary marker to increase the specificity and/or sensitivity of the well-established fecal immunochemical test (FIT) in CRC screening.
4

Samba-Louaka, Ascel, Jean-Philippe Nougayrède, Claude Watrin, Eric Oswald e Frédéric Taieb. "The Enteropathogenic Escherichia coli Effector Cif Induces Delayed Apoptosis in Epithelial Cells". Infection and Immunity 77, n. 12 (28 settembre 2009): 5471–77. http://dx.doi.org/10.1128/iai.00860-09.

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ABSTRACT The cycle inhibiting factor (Cif) belongs to a family of bacterial toxins, the cyclomodulins, which modulate the host cell cycle. Upon injection into the host cell by the type III secretion system of enteropathogenic Escherichia coli (EPEC), Cif induces both G2 and G1 cell cycle arrests. The cell cycle arrests correlate with the accumulation of p21waf1 and p27kip1 proteins that inhibit CDK-cyclin complexes, whose activation is required for G1/S and G2/M transitions. Increases of p21 and p27 levels are independent of p53 transcriptional induction and result from protein stabilization through inhibition of the ubiquitin/proteasome degradation pathway. In this study, we show that Cif not only induces cell cycle arrest but also eventually provokes a delayed cell death. Indeed, 48 h after infection with EPEC expressing Cif, cultured IEC-6 intestinal cells were positive for extracellular binding of annexin V and exhibited high levels of cleaved caspase-3 and lactate dehydrogenase release, indicating evidence of apoptosis. Cif was necessary and sufficient for inducing this late apoptosis, and the cysteine residue of the catalytic site was required for Cif activity. These results highlight a more complex role of Cif than previously thought, as a cyclomodulin but also as an apoptosis inducer.
5

Hsu, Yun, Gregory Jubelin, Frédéric Taieb, Jean-Philippe Nougayrède, Eric Oswald e C. Erec Stebbins. "Structure of the Cyclomodulin Cif from Pathogenic Escherichia coli". Journal of Molecular Biology 384, n. 2 (dicembre 2008): 465–77. http://dx.doi.org/10.1016/j.jmb.2008.09.051.

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6

Canizalez-Roman, Adrian, Juan E. Reina-Reyes, Uriel A. Angulo-Zamudio, Eloy E. Geminiano-Martínez, Antonio F. Flores-Carrillo, Rolando R. García-Matus, Norma M. Valencia-Mijares et al. "Prevalence of Cyclomodulin-Positive E. coli and Klebsiella spp. Strains in Mexican Patients with Colon Diseases and Antimicrobial Resistance". Pathogens 11, n. 1 (23 dicembre 2021): 14. http://dx.doi.org/10.3390/pathogens11010014.

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Colon diseases, such as colorectal cancer (CRC), are multifactor diseases that affect more than one million people per year; recently, the microbiota has been associated with an etiologic factor, specifically bacterial cyclomodulin positivity (CM+). Unfortunately, there are no studies from Mexico that detail the presence of bacterial CM+ in patients with colon diseases. We therefore performed a comprehensive study to investigate the associations and prevalence of cyclomodulin-positive Diarrheagenic E. coli (DEC), non-DEC, and Klebsiella spp. strains isolated from Mexican subjects with colon diseases. In this work, we analyzed 43 biopsies, 87 different bacteria were isolated, and E. coli was the most frequently noted, followed by Klebsiella spp., and Enterococcus spp. E. coli, non-DEC, and EPEC belonging to phylogroup B2 were the most prevalent. More than 80% of E. coli and Klebsiella were CM+. pks, cdt, cnf, and cif were identified. cdt was associated with non-DEC, cif and its combinations with EPEC, as well as cdt and psk with Klebsiella. Lastly, all the CM+ bacteria were resistant to at least one antibiotic (34% were MDR, and 48% XDR). In conclusion, the high prevalence of bacterial CM+ in colon disease patients suggests that these bacteria play an important role in the genesis of these diseases.
7

Toro, Tasha B., Julia I. Toth e Matthew D. Petroski. "The Cyclomodulin Cycle Inhibiting Factor (CIF) Alters Cullin Neddylation Dynamics". Journal of Biological Chemistry 288, n. 21 (15 aprile 2013): 14716–26. http://dx.doi.org/10.1074/jbc.m112.448258.

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8

Buc, Emmanuel, Damien Dubois, Pierre Sauvanet, Jennifer Raisch, Julien Delmas, Arlette Darfeuille-Michaud, Denis Pezet e Richard Bonnet. "High Prevalence of Mucosa-Associated E. coli Producing Cyclomodulin and Genotoxin in Colon Cancer". PLoS ONE 8, n. 2 (14 febbraio 2013): e56964. http://dx.doi.org/10.1371/journal.pone.0056964.

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9

Chavez, Carolina Varela, Grégory Jubelin, Gabriel Courties, Aurélie Gomard, Nadège Ginibre, Sylvie Pages, Frédéric Taïeb et al. "The cyclomodulin Cif of Photorhabdus luminescens inhibits insect cell proliferation and triggers host cell death by apoptosis". Microbes and Infection 12, n. 14-15 (dicembre 2010): 1208–18. http://dx.doi.org/10.1016/j.micinf.2010.09.006.

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10

Samba-Louaka, Ascel, Jean-Philippe Nougayrède, Claude Watrin, Grégory Jubelin, Eric Oswald e Frédéric Taieb. "Bacterial cyclomodulin Cif blocks the host cell cycle by stabilizing the cyclin-dependent kinase inhibitors p21waf1and p27kip1". Cellular Microbiology 10, n. 12 (dicembre 2008): 2496–508. http://dx.doi.org/10.1111/j.1462-5822.2008.01224.x.

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Ti possono interessare anche gli elenchi estesi di opere sul tema "Cyclomodulin":
Articoli di riviste

Tesi sul tema "Cyclomodulin":

1

Mambu, Julien. "Dérégulation de la prolifération cellulaire par Salmonella Typhimurium et implication dans la pathogenèse". Electronic Thesis or Diss., Tours, 2020. http://www.theses.fr/2020TOUR5023.

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L’entéropathogène Salmonella Typhimurium a été mis en cause dans la dérégulation la prolifération cellulaire au niveau de l’intestin après infection. Toutefois, le mécanisme mis en jeu reste peu connu. Salmonella Typhimurium, exprime à sa surface une invasine, Rck, qui interagit et active le récepteur de l’EGF (EpidermalGrowth Factor) à la surface de la cellule cible, conduisant à l’internalisation de la bactérie. Sachant que l’activation du récepteur de EGF régule des processus cellulaires incluant la prolifération-différentiation, ma thèse avait pour objectif de déterminer l’impact de Rck sur la prolifération de cellules épithéliales intestinales et son implication dans la pathogenèse. La prolifération cellulaire est régulée au niveau des quatre phases du cycle cellulaire. Par un approche in vitro, nous avons démontré que Rck manipule le cycle cellulaire en causantun ralentissement de la progression en phase S du cycle cellulaire, phase de réplication de l’ADN. Cette modulation du cycle s’accompagnait de l’apparition de dommages à l’ADN dans les cellules infectées. Par l’inhibition des voies de réponse aux dommages à l’ADN, nous avons démontré que la modulation du cycle cellulaire induite par Rck est une conséquence de l’activation de ces voies. Finalement, nous avons démontré que Rck manipule le cycle cellulaire de la cellule hôte afin de favoriser l’internalisation d’autres bactéries exprimant Rck. Ces résultats suggèrent un nouveau mécanisme utilisé par Salmonella pour détourner les mécanismes cellulaires de l’hôte afin de créer un environnement favorable pour la colonisation intestinale
The enteropathogen Salmonella Typhimurium has been implicated in the deregulation of cell proliferation in the intestine after infection. However, the mechanism involved remains poorly understood. Salmonella Typhimurium expresses on its surface an invasin, Rck, which interacts with and activates the epidermal growth factor receptor (EGFR) on the surface of the target cell, leading to the internalization of the bacteria. Knowing that EGFR activation regulates cellular processes including proliferation-differentiation, my thesis aimed to determine the impact of Rck on the proliferation of intestinal epithelial cells and its involvement in pathogenesis. Cell proliferation is regulated within the four phases of the cell cycle. By using an in vitro approach, we showed that Rck manipulates the cell cycle by delaying its progression in the S phase, the DNA replication phase. This modulation of the cycle was accompanied by the appearance of DNA damage in infected cells. By inhibiting the DNA damage response pathways, we have demonstrated that Rck-induced cell cycle modulation is a consequence of the activation of these pathways. Finally, we demonstrated that Rck-mediated manipulation of the host cell cycle facilitates the internalization of other bacteria expressing Rck. These results suggest a new mechanism used by Salmonella to hijack host cellular mechanisms to create a suitable environment for intestinal colonization
2

Varela, Chavez Carolina. "Caractérisation fonctionnelle d’une cyclomoduline pro-apoptotique nommée Cif (Cycle Inhibiting Factor) chez les bactéries entomopathogènes du genre Photorhabdus". Montpellier 2, 2009. http://www.theses.fr/2009MON20183.

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3

Noto, Benjamin [Verfasser], e M. Alexander [Akademischer Betreuer] Schmidt. "Transport des Cyclomodulins Cif in eukaryotische Zellen mit Hilfe von "Cell penetrating peptides" / Benjamin Noto ; Betreuer: M. Alexander Schmidt". Münster : Universitäts- und Landesbibliothek Münster, 2013. http://d-nb.info/1141383748/34.

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4

Raisch, Jennifer. "Piste infectieuse à Escherichia coli toxinogènes dans le cancer colorectal". Thesis, Clermont-Ferrand 1, 2014. http://www.theses.fr/2014CLF1MM09/document.

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Le cancer colorectal (CCR) est au 3ème rang des cancers les plus répandus dans le monde. Il est bien établi que l'inflammation est un acteur clé de la carcinogenèse colorectale. Parmi les cellules de l'infiltrat inflammatoire tumoral, les macrophages jouent un rôle moteur dans la carcinogenèse en sécrétant un arsenal de cytokines/chimiokines et facteurs protumoraux tels que la prostaglandine E2 (PGE2), produit enzymatique de la cyclo-oxygénase 2 (COX-2). Des dysbioses du microbiote intestinal, en particulier une augmentation d’Escherichia coli (E. coli) appartenant au phylogroupe B2 et producteurs de cyclomodulines ont été rapportées chez les patients atteints de CCR. Mon doctorat s'inscrit dans lacaractérisation du potentiel carcinogène de souches d'E. coli B2 isolées de patients atteints de CCR, et ceci notamment au travers de leur interaction avec les macrophages, principale population de l'infiltrat inflammatoire tumoral. La caractérisation de souches d'E. coli de phylogroupe B2 isolées de patients atteints de CCR a révélé qu'elles possèdent de faibles capacités d'adhésion et d'invasion aux cellulesépithéliales intestinales comparativement à la souche adhérente et invasive d'E. coli LF82. En revanche, les E. coli associés au CCR sont capables d'induire l'expression du récepteur CEACAM6 par les cellules épithéliales coliques humaines T-84. Nous avons également montré que la souche d'E. coli 11G5 associée au CCR est capable, dans un modèle murin d'infection chronique exprimant CEACAM6, de coloniser la muqueuse colique, d'induire une inflammation colique et des dommages épithéliaux, ainsi qu'une augmentation de la prolifération cellulaire, suggérant que les E. coli associés au CCR pourraient participer à l'établissement d'un épithélium hyperprolifératif. Par ailleurs, nous avons montré que les E. coli isolés de patients atteints de CCR sont capables de survivre en macrophages humains THP-1, suggérant que les macrophages pourraient représenter un niche de réplication pour ces bactéries. Les souches d'E. coli isolées de CCR sont capables d'induire des niveaux de COX-2 significativement supérieur à celui induit par une souche de la souche d'E. coli commensale ED1a. L'expression de COX-2 induite par les souches d'E. coli associées au CCR est dépendante du nombre et de la viabilité des bactéries internalisées. Enfin, l'analyse des voies de signalisation a révélé que la voie de signalisation p38 permet de contrôler le nombre de bactéries intracellulaires et l'expression de COX-2, suggérant que cette voie de signalisation pourrait être impliquée dans la survie et la multiplication des E. coli associés au CCR. Ce travail de thèse a contribué à une meilleure caractérisation des souches d'E. coli associés au cancer du côlon et a ouvert de nouvelles pistes sur la compréhension de leurcapacité à influencer la carcinogenèse colorectale. Plus largement, ces données suggèrent que les bactéries associées aux tumeurs pourraient jouer un rôle actif dans la progression tumorale, et ceci notamment au travers de leur interaction avec les macrophages. En plus d'être une cible, le tropisme particulier des E. coli associés au CCR pour les macrophages en ferait de bons candidats pour le développement de nouvelles stratégies thérapeutiques
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